Sensitivity of CT perfusion for the diagnosis of cerebral infarction

We aimed to determine the sensitivity of CT perfusion (CTP) for the diagnosis of cerebral infarction in the acute stage. We retrospectively reviewed patients with ischemic stroke who underwent brain CTP on arrival and MRI-diffusion weighted image (DWI) after hospitalization between October 2008 and October 2011. Final diagnosis was made from MRI-DWI findings and 87 patients were identified. Fifty-five out of 87 patients (63%) could be diagnosed with cerebral infarction by initial CTP. The sensitivity depends on the area size (s) : 29% for S<3 cm2, 83% for S≥3 cm2-<6 cm2, 88% for S≥6 cm2-<9 cm2, 80% for S≥9 cm2-<12 cm2, and 96% for S≥12 cm2 (p<0.001). Sensitivity depends on the type of infarction : 0% for lacunar, 74% for atherothrombotic, and 92% for cardioembolism (p<0.001). Sensitivity is not correlated with hours after onset. CT perfusion is an effective imaging modality for the diagnosis and treatment decisions for acute stroke, particularly more serious strokes

Effect of a pharmacological inhibition of a T cell function on IA progression.

<p>(A) Dose-dependent suppression of Concanavalin A-induced IL-2 production by Cyclosporine A <i>in vivo</i>. F344/Jcl rats were treated with each dose of Concanavalin A (n = 3) or Cyclosporine A combined with 15 mg/kg Concanavaline A (n = 3). Before administration (pre) or after 3 h (post), serum samples were prepared from rats and IL-2 concentration in these samples was examined by ELISA. Noted that 15 mg/kg Cyclosporine A almost completely suppressed Concanavalin A-induced IL-2 production. (B) Failure of suppression of IA progression, degenerative changes and infiltration of macrophages in lesions by treatment with Cyclosporine A. F344/Jcl rats were subjected to IA induction and, at 14^th day after the induction, slices from IA specimen induced at ACA-OA bifurcation were prepared for further analyses. Administration of Cyclosporine A was started 1 day before the induction and lasted for a whole experimental period (15 mg/kg, once a day). Systemic blood pressure was evaluated before sacrifice without any anesthesia. Area of induced IAs (Vehicle; n = 8, Cyclosporine A; n = 8) and distance between disrupted internal elastic lamina (IEL) in lesions were evaluated after Elastica van Gieson (EvG) staining (Representative images are shown in upper left panels). Degenerative change in IA walls was assessed by thickness of medial smooth muscle cell layer after immunostaining for α-smooth muscle actin. Number of infiltrated macrophages in IA lesions was evaluated after immunostaining for a macrophage marker CD68 (per 12,100 μm²). Data represents mean ± SEM. Representative images of immunostaining for CD68 (green) and α-smooth muscle actin (α-SMA, red) and of nuclear staining DAPI (blue) are shown in lower left panels. Bar, 20 μm.</p

Proper macrophage activation in a T cell-deficient F344/NJcl-rnu/rnu rat.

<p>Bone marrow macrophages (BMMs) were prepared from a T cell-deficient F344/NJcl-rnu/rnu rat and a wild type F344/Jcl rat as described in Materials and Methods in detail. Phagocytic activity (A) and response to inflammatory stimulation with LPS (B, C) of BMMs prepared were then evaluated. To examine phagocytic activity, BMMs from both strains were treated with iron-containing nanoparticles, Ferumoxytol, for 24 h and engulfed particles were detected by Berlin blue staining (A). Bar, 20 μm. Response of BMMs from both strains to LPS was assessed by Western blot analysis and RT-PCR analyses targeting NF-κB-regulated pro-inflammatory genes. For Western blotting, BMMs were stimulated with LPS (1 μg/ml) for indicated time period and total cell lysate prepared from these stimulated cells was subjected to Western blotting for IκBα, phosphorylated form of p65 subunit (s536, p-p65) and p65 subunit to evaluate NF-κB activation, using Western blotting for α-tubulin as an internal control. For RT-PCR analyses, total RNA was purified from stimulated cells (LPS 0.1, 1, 10 μg/ml, 60 min) and subjected to RT-PCR analyses for MCP-1 (<i>Ccl2</i>), TNF-α (<i>Tnf</i>) and COX-2 (<i>Ptgs2</i>) after reverse transcription. Data represents mean ± SEM (n = 4). Noted that BMMs from a T cell-deficient rat shows a similar phagocytic activity and properly responses to inflammatory stimulation as in a wild type BMMs.</p

Accumulation of T cells in human unruptured IA walls.

<p>(A, B) Accumulation of CD3-, CD4- and CD8-positive T cells in human unruptured IA walls. Adjacent sections were prepared from branches of carotid artery (Control) or unruptured IA lesion (Aneurysm) of humans and immunostained for a T cell marker, CD3, or subset specific makers, CD4 and CD8, respectively. Box in (A) indicates the region magnified in the following panels shown in (B). Bar, 100 μm. (C) Number of CD3-, CD4- and CD8-positive T cells in control arterial walls and IA walls. Data represents mean ± SEM (n = 10 in control, n = 15 in aneurysm). *, p<0.05, **, p<0.01 in a Mann−Whitney U test. Noted the significant increase in both CD4- and CD8-positive T cells in IA walls compared with those in control arterial walls.</p

Abstract Number ‐ 56: Investigation of Aneurysmal Initiation Factor with Experimental Animal Model by Computational Fluid Dynamics Analysis

Introduction Hemodynamics has been reported to be involved in the pathophysiology of the initiation of intracranial aneurysms. Computational fluid dynamics (CFD) simulation has been widely used to investigate what kind of hemodynamics is related to intracranial aneurysm development or rupture. However, in the case of humans, it is difficult to obtain cerebrovascular images before the aneurysm formation because most of them are detected incidentally by magnetic resonance angiography (MRA) or computed tomography angiography (CTA). Therefore, the mechanism of aneurysm initiation has not been elucidated yet. In this study, CFD analysis was conducted with experimental animal models. Furthermore, immunostainings and Elastica van Gieson (EvG) staining were also performed to investigate the relationship between hemodynamics and aneurysm initiation. Methods We selected the experimental aneurysm model of a rat proposed by Shimizu et al.[1] With this model, aneurysms can be induced with a certain probability at the artificial bifurcation site created by end‐to‐side anastomosis of bilateral common carotid arteries and induced hypertension. Among the 50 rats surgically manipulated, 5 de novo cases and 14 cases without aneurysm initiation defined as stable cases were included in this study. The other 31 cases were excluded because of death or lack of imaging quality. MRA was conducted weekly until 4 weeks after manipulation. Acquired images were processed for the CFD analysis and various kinds of hemodynamic parameters were calculated. Among them, we regarded dimensionless wall shear stress divergence (WSSD*) and pressure loss coefficient (PLc) as the hemodynamic parameters previously suggested to be related to aneurysm initiation[2]. Vessels were collected after 2 weeks of follow‐up, and we observed endothelial cells (EC), smooth muscle cells (SMC), and the internal elastic lamina (IEL) at the apex of the bifurcationby immunostaining and EvG staining. Results The CFD results showed that a high WSSD* area existed at the apex of bifurcation in both de novo cases and stable cases. The averaged WSSD* of the de novo cases was 18.2% higher than that of the stable cases (de novo: 0.577 ± 0.243, stable: 0.488 ± 0.235). Likewise, the average PLc of the de novo cases was 11.5% higher than that of the stable cases (de novo: 8.22 ± 1.76, stable: 7.37 ± 2.49). The immunostaining images demonstrated that EC and SMC were more degenerated in de novo cases than in stable cases. Furthermore, the EvG staining images showed that IEL degenerated only in the de novo cases. Therefore, because WSSD* and PLc indicate a stretching force and flow impingement on the vessel wall, respectively, the elevation of those parameters may contribute to damage of EC, SMC, and IEL known as pathological features of an intracranial aneurysm. Conclusions CFD analysis and tissue observation were conducted with the vessels of the experimental animal model (5 de novo cases and 14 stable cases). Our results indicate that high WSSD* and high PLc are the factors related to aneurysm initiation

Polarimetric performance of Si/CdTe semiconductor Compton camera

A Compton camera has been developed based on Si and CdTe semiconductor detectors with high spatial and spectral resolution for hard X- and gamma-ray astrophysics applications. A semiconductor Compton camera is also an excellent polarimeter due to its capability to precisely measure the Compton scattering azimuth angle, which is modulated by linear polarization. We assembled a prototype Compton camera and conducted a beam test using nearly 100% linearly polarized gamma-rays at SPring-8

Characterization of Nutrient Intake in Biopsy-Confirmed NAFLD Patients

Objectives: Weight loss improves the liver pathophysiological status of nonalcoholic fatty liver disease (NAFLD) patients. However, there are few studies that investigate the accurate relationships between nutritional intake and disease progression in NAFLD patients. Methods: A total of 37 biopsy-confirmed NAFLD patients were enrolled in this study. Clinical and nutritional control data of 5074 persons were obtained from the National Institute of Health and Nutrition. Each NAFLD subject recorded dietary intake for seven consecutive days using a dietary questionnaire and photographs of each meal. A dietitian analyzed and quantified the nutritional data in each patient. We further analyzed the nutritional intake of NAFLD patients in three groups according to the following criteria: (1) liver fibrosis degree (advanced, early), (2) gender (male, female), and (3) body mass index (BMI) (high, low). Results: Excesses or deficiencies of multiple nutrients were found in NAFLD patients compared with control subjects. In addition, there were variations in nutritional intake. (1) The intake of vitamins A, B6, and E, pantothenic acid, soluble dietary fiber, and salt was lower in the advanced fibrosis group than in the early fibrosis group. (2) Fat intake was higher in male patients, and dietary fiber intake was lower in both male and female patients compared with control subjects. (3) Saturated fatty acid intake was higher, and copper and vitamin E intakes were lower in patients with high BMI than with low BMI. Conclusions: Our study demonstrates that differences were found in some nutrient intake of NAFLD patients and controls and according to the severity of the conditions (liver fibrosis degree, BMI)